Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer Export

@article{citeulike:3199844, abstract = {Comparative genomic hybridization (CGH) was used to screen for genomic imbalances in 24 exocrine pancreatic carcinomas, including 11 low-passage cell lines (4-8 subcultures) and 13 uncultured samples. Aberrations were found in all cell lines and in seven of the 13 biopsies. The most frequent changes in the cell lines were gains of 20q (91\%), 11q (64\%), 17q (64\%), 19q (64\%), 8q, 12p, 14q, and 20p (55\%), and losses of 18q (100\%), 9p (91\%), 15q (73\%), 21q (64\%), 3p (55\%), and 13q (55\%). High-level gains (tumor to normal ratio over 1.5) were detected at 3q, 6p, 7q, 8q, 12p, 19q, and 20q. Among the tumor biopsies, overrepresentations of 7p and 8q were most common (31\%), followed by 5p, 5q, 11p, 11q, 12p, and 18q (23\%), whereas the most frequent losses involved 18p and 18q (31\%) and 6q and 17p (23\%). The genetic changes in nine samples obtained from metastatic lesions did not differ significantly from those in 15 primary carcinomas. Most of the gains and losses detected in this CGH study correspond well to those identified in previous cytogenetic and molecular genetic investigations of pancreatic carcinomas. However, frequent gain of 12p and loss of 15q have not been previously reported. Molecular genetic analyses of these chromosome arms are warranted, and may lead to the discovery of novel genes important in pancreatic carcinogenesis. Genes Chromosomes Cancer 20:383-391, 1997. {\copyright} 1997 Wiley-Liss, Inc.}, address = {Laboratory of Cancer Genetics, Tampere University Hospital and Institute of Medical Technology, University of Tampere, Tampere, Finland; Department of Clinical Genetics, University Hospital, Lund, Sweden; Department of Pathology and Cytology, University Hospital, Lund, Sweden; Department of Surgery, University Hospital, Lund, Sweden; Laboratory of Cancer Genetics, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland}, author = {Mahlam\"{a}ki, Eija H. and H\"{o}glund, Mattias and Gorunova, Ludmila and Karhu, Ritva and Dawiskiba, Sigmund and Andr\'{e}n-Sandberg, \r{A}ke and Olli-P and Johansson, Bertil}, citeulike-article-id = {3199844}, citeulike-linkout-0 = {http://dx.doi.org/10.1002/(SICI)1098-2264(199712)20:4%3C383::AID-GCC10%3E3.0.CO;2-O}, citeulike-linkout-1 = {http://www3.interscience.wiley.com/cgi-bin/abstract/55566/ABSTRACT}, doi = {10.1002/(SICI)1098-2264(199712)20:4%3C383::AID-GCC10%3E3.0.CO;2-O}, journal = {Genes, Chromosomes and Cancer}, keywords = {20q, cancer, pancreatic}, number = {4}, pages = {383--391}, posted-at = {2008-09-06 17:38:46}, priority = {2}, title = {Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer}, url = {http://dx.doi.org/10.1002/(SICI)1098-2264(199712)20:4%3C383::AID-GCC10%3E3.0.CO;2-O}, volume = {20}, year = {1997} }

TY - JOUR ID - citeulike:3199844 L3 - citeulike-article-id:3199844 N2 - Comparative genomic hybridization (CGH) was used to screen for genomic imbalances in 24 exocrine pancreatic carcinomas, including 11 low-passage cell lines (4-8 subcultures) and 13 uncultured samples. Aberrations were found in all cell lines and in seven of the 13 biopsies. The most frequent changes in the cell lines were gains of 20q (91%), 11q (64%), 17q (64%), 19q (64%), 8q, 12p, 14q, and 20p (55%), and losses of 18q (100%), 9p (91%), 15q (73%), 21q (64%), 3p (55%), and 13q (55%). High-level gains (tumor to normal ratio over 1.5) were detected at 3q, 6p, 7q, 8q, 12p, 19q, and 20q. Among the tumor biopsies, overrepresentations of 7p and 8q were most common (31%), followed by 5p, 5q, 11p, 11q, 12p, and 18q (23%), whereas the most frequent losses involved 18p and 18q (31%) and 6q and 17p (23%). The genetic changes in nine samples obtained from metastatic lesions did not differ significantly from those in 15 primary carcinomas. Most of the gains and losses detected in this CGH study correspond well to those identified in previous cytogenetic and molecular genetic investigations of pancreatic carcinomas. However, frequent gain of 12p and loss of 15q have not been previously reported. Molecular genetic analyses of these chromosome arms are warranted, and may lead to the discovery of novel genes important in pancreatic carcinogenesis. Genes Chromosomes Cancer 20:383-391, 1997. © 1997 Wiley-Liss, Inc. IS - 4 JF - Genes, Chromosomes and Cancer AD - Laboratory of Cancer Genetics, Tampere University Hospital and Institute of Medical Technology, University of Tampere, Tampere, Finland; Department of Clinical Genetics, University Hospital, Lund, Sweden; Department of Pathology and Cytology, University Hospital, Lund, Sweden; Department of Surgery, University Hospital, Lund, Sweden; Laboratory of Cancer Genetics, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland EP - 391 TI - Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer VL - 20 SP - 383 KW - 20q KW - cancer KW - pancreatic AU - Mahlamäki, Eija AU - Höglund, Mattias AU - Gorunova, Ludmila AU - Karhu, Ritva AU - Dawiskiba, Sigmund AU - Andrén-Sandberg, Åke AU - Olli-P AU - Johansson, Bertil PY - 1997/// UR - http://dx.doi.org/10.1002/(SICI)1098-2264(199712)20:4%3C383::AID-GCC10%3E3.0.CO;2-O ER -